1. Field of the Invention
The invention relates to the use of nitrous oxide (N2O) or of an N2O donor for producing all or part of a medicinal product intended to treat or prevent post-ischemic brain cell deterioration, in particular deterioration subsequent to a stroke, especially all or part of an inhalable gaseous medicinal product, in humans or animals.
2. Related Art
In cerebral ischemia subsequent to a stroke, and in strokes in general, a functional alteration of many neurotransmission systems is usually noted from a neurochemical point of view, in particular an increase in the release of glutamate, the excitotoxicity and contribution of which to neuronal death are known, as recalled by Dirnagl et al., Trends Neurosci, 22: 391, 1999.
Moreover, from a functional point of view, in the case of global ischemia in the rat, an increase is observed in locomotor activity, in particular described by Wang and Corbett, Brain Res., 533: 78, 1990; Baldwin et al., Neurodegeneration 2: 139, 1993, the development of which is generally attributed to an alteration in cognitive functions of spatial recognition rather than to an alteration in sensory-motor functions.
As a result, a potential therapeutic role for ionotropic and metabotropic glutamergic receptor antagonists have been suspected, in particular by Chazot, Curr Opin Invest Drugs 1: 370, 2000; Drian et al., Neurochem Int 38: 509, 2001.
It also appears that the deleterious effects of known cerebral ischemias appear to involve localized ischemias which are thought to be caused by glutamergic excitotoxicity.
In fact, the therapeutic potential of glutamergic receptor antagonists is often put forward in the treatment of neuropathologies of excitotoxic origin, in particular cerebral ischemia, as described by Dirnagl et al., Trends Neurosci 22: 391, 1999, and productive disorders, as described by Benes, Brain Res. Review 31: 251, 2000.
However, the physiology of glutamergic receptors is complex and it appears that the high affinity antagonists may also exhibit neurotoxic properties, according to Burns et al., Psychopharmacology 115: 516, 1994.
Thus, a potential therapeutic advantage of low affinity antagonists, in particular for NMDA, has recently been proposed by Palmer and Widzowski, Amino acids 19: 151, 2000.
Moreover, document WO-A-02/09731 is also known, which relates to the use of CO, optionally supplemented with another gas, for treating inflammations of the upper respiratory tracts or of the bronchi. That document therefore targets the treatment of pathologies such as asthma, cystic fibrosis, pneumopathies or the like.
In addition, document EP-A-861672 teaches a method of treatment which can be used in emergency situations by administering various gases. However, this does not relate to post-ischemic brain cell degradations subsequent to strokes.
Finally, document FR-A-2812545 teaches a combination of gas and active product intended to treat or prevent pain. The active product is an analgesic, an anti-inflammatory, an anti-pyretic or the like.